Other Seminars

Professor Dominic Kwiatkowski, Dr Gavin Band

The third seminar of the series will be hosted by Professor Dominic Kwiatkowski. He will be speaking on, "Translating genomic data into actionable information for malaria control".
Dr Gavin Band will talk on, “Heterogeneity and structural variation in the host genetic basis of severe malaria”... Read more

The third seminar of the series will be hosted by Professor Dominic Kwiatkowski. He will be speaking on, "Translating genomic data into actionable information for malaria control".
Dr Gavin Band will talk on, “Heterogeneity and structural variation in the host genetic basis of severe malaria” and Alistair Miles, “Extreme genetic diversity: challenges and opportunities for mosquito control in Africa”.

Peiter Eichhorn

Protein modification by ubiquitination has emerged as a critical regulatory event in virtually all aspects of cell biology. Ubiquitination is a reversible process, and ubiquitin moieties can be removed from polypeptides by deubiquitinating enzymes (DUBs). Using a shRNA deubiquitinating enzyme... Read more

Protein modification by ubiquitination has emerged as a critical regulatory event in virtually all aspects of cell biology. Ubiquitination is a reversible process, and ubiquitin moieties can be removed from polypeptides by deubiquitinating enzymes (DUBs). Using a shRNA deubiquitinating enzyme library we have sought to understand the role of deubiquitinating enzymes in cancer progression with the goal to identify novel mechanistic biomarkers that predict response to targeted therapies presently being used in the clinic. This presentation will show some of our most recent findings including our work on the identification of a number of deubiquitinating enyzmes involved in vemurafenib resistance in BRAF mutant melanoma. In addition, we have identified the deubiquitinating enzymes USP15 and USP26 as novel modulators of the TGF-beta pathway and critical factors in glioblastoma pathogeneisis. I will provide a brief summary on both of these stories and the present work that we are doing in my lab.
Biography:
Dr. Pieter Eichhorn is a group leader at the Cancer Science Institute of Singapore. He holds a bachelor of science degree specializing in human genetics from the University of Western Ontario. He did his Ph.D. work under the direction of Prof. Tom Strachan at the University of Newcastle upon Tyne, focusing on cloning of the gene for Cornelia de Lange syndrome. He then did his postgraduate studies with Rene Bernards at the Netherlands Cancer Institute, Amsterdam, where he performed some of the first RNAi screens in mammalian cells that led to the identification of the PP2A subunit PR55 gamma as a potent inhibitor of the oncogene c-SRC. In 2006 he joined the lab of Jose Baselga at Vall d’Hebron Institute of Oncology, Barcelona, where he continued utilizing genome wide technologies to identify novel genes in cancer relevant pathways, including work that led to the identification of PI3K hyperactivation in Lapatinib resistance. In 2010 he became a faculty member at Massachusetts General Hospital and Harvard Medical School where he identified both cyclin E and RSK4 as mechanisms of resistance to Trastuzumab and PI3K inhibitors, respectively. Since joining the Cancer Science Institute, Pieter’s research is mostly focused on the role deubiquitinating enzymes in the TGFβ pathway and the identification of factors involved in targeted therapeutic resistance.

Dr Kamal Patel

Assistant Professor Don Conrad

Male gametogenesis is a fascinating biological system which offers numerous research opportunities at the intersection of medicine, evolution, and genome biology. In this seminar I will discuss our ongoing work to develop genome sequencing into a useful diagnostic assay for the clinical management... Read more

Male gametogenesis is a fascinating biological system which offers numerous research opportunities at the intersection of medicine, evolution, and genome biology. In this seminar I will discuss our ongoing work to develop genome sequencing into a useful diagnostic assay for the clinical management of male infertility. This work has inspired the development of novel statistical approaches to identify potential disease causing genotypes from n=1 cases of infertility, as well as novel experimental methods to validate these variants in vivo.

Professor Kang Zhang

Kang Zhang, MD, PhD is the founding director of Institute for Genomic Medicine, Co-Director of BioMaterials and Tissue Engineering Center at Institute of Engineering in Medicine, Chief of Ophthalmic Genetics, Professor of Ophthalmology and Genetics at University of California San Diego. Dr. Zhang... Read more

Kang Zhang, MD, PhD is the founding director of Institute for Genomic Medicine, Co-Director of BioMaterials and Tissue Engineering Center at Institute of Engineering in Medicine, Chief of Ophthalmic Genetics, Professor of Ophthalmology and Genetics at University of California San Diego. Dr. Zhang obtained his M.D. with Magna Cum Laude honours from Harvard Medical School and MIT joint MD program and his PhD in genetics from Harvard University. He did his postdoctoral training also at Harvard. He completed his residency in ophthalmology at Johns Hopkins University and his retina fellowship at University of Utah. He was a faculty member at Johns Hopkins University, Cleveland Clinic Foundation, and the University of Utah.
Among his honours include AAAS fellow, AIBME fellow, memberships in Association of American Physicians and American Society of Clinical Investigation, Outstanding Achievement Award of Chinese Ophthalmological Society, Chang Jiang Scholar, Burroughs Wellcome Fund Clinical Scientist Award in Translational Research; Lew R. Wasserman Merit Award and Senior Investigator Award from Research to Prevent Blindness; Charles Schepens Award for Excellence in Retina Research; and Johns Hopkins Medical Institutions Clinician Scientist Award. He has numerous grants from National Institute of Health including an NIH Director’s Transformative RO1 and other foundation grants. Dr. Zhang has published over 160 peer-reviewed manuscripts in top peer-reviewed journals- covering a wide range of topics in genetics, epigenetics, stem cells, nano-engineering and 3D printing, and clinical trials. His discovery that HTRA1 is a major susceptibility gene for age-related macular degeneration is listed as one of “top-ten breakthroughs in 2006” by Science.

Dr Chris Foley

In Genome Wide Association Studies the relationship between a phenotype, with discrete outcome levels, and a genotype is typically assessed via linear regression, which necessarily ignores the non-normality of the outcome. Motivated by this, we consider a transformation that connects the linear... Read more

In Genome Wide Association Studies the relationship between a phenotype, with discrete outcome levels, and a genotype is typically assessed via linear regression, which necessarily ignores the non-normality of the outcome. Motivated by this, we consider a transformation that connects the linear effects to the non-linear scale. The approach improves on current transformations by maintaining small bias, of the non-linear genetic effect estimate, when variation in the outcome is explained mainly by additional covariates, e.g. age and gender.
As an example, we consider a binary trait and several genetic and non-genetic predictors connected via a logit link-function. The method, however, is applicable to a wide class of non-normal phenotypes and link-functions.

Prof Marina Botto

Marina Botto FMedSci is the Director of the Centre for Complement and Inflammation Research (CCIR) and Professor of Rheumatology at the Imperial College London. She is also a Consultant Rheumatologist at Imperial Academic Health Science Centre, Hammersmith Campus.
The focus of her research... Read more

Marina Botto FMedSci is the Director of the Centre for Complement and Inflammation Research (CCIR) and Professor of Rheumatology at the Imperial College London. She is also a Consultant Rheumatologist at Imperial Academic Health Science Centre, Hammersmith Campus.
The focus of her research programme is to understand how complement deficiency contributes to the autoimmune disease, systemic lupus erythematosus (SLE). Her laboratory is particularly interested in understanding the consequences of inherited complement deficiencies in humans and the role(s) that the complement system plays in the clearance of dying cells as well as immune complexes. Using in vivo models, genetic and cellular approaches and experimental models of inflammation she has demonstrated that: i) inherited defects in the pathways for clearance of cellular debris and immune complexes predispose to the development of SLE; ii) there is a link between spontaneous autoimmunity and abnormalities of the physiological clearance of apoptotic cells in humans with complement deficiency; iii) the complement system modulates the adaptive immune system; iv) autoimmunity varies according to the genetic background of the model used and identified lupus susceptibility loci. The laboratory currently aims to delineate the contribution of complement system in the induction and resolution of inflammation and to define the mechanisms by which the complement system regulates the tolerance to self-antigens.

Dr. David Brough

Inflammation contributes to the progression of Alzheimer’s disease (AD). On-going research is establishing the NLRP3-inflammasome complex as one of the most important regulators of inflammation in AD. The NLRP3 inflammasome forms a molecular platform inside microglia catalysing the activation of... Read more

Inflammation contributes to the progression of Alzheimer’s disease (AD). On-going research is establishing the NLRP3-inflammasome complex as one of the most important regulators of inflammation in AD. The NLRP3 inflammasome forms a molecular platform inside microglia catalysing the activation of the protease caspase-1. Caspase-1 is responsible for converting the potent pro-inflammatory cytokine interleukin-1β (IL-1β) from an inactive to an active secreted form. Active caspase-1 is present in the brains of humans with AD, suggesting that NLRP3 may contribute to the human condition. NLRP3 is also central to the development of inflammation, pathology and memory deficits in a mouse model of AD. Anti-IL-1 drugs such as the biologicals canakinumab and anakinra do not easily penetrate the brain and there are no molecules known to directly target NLRP3 in clinical use. We found that NSAIDs of the fenamate class were effective and selective inhibitors of the NLRP3 inflammasome via inhibition of the volume regulated anion channel (VRAC) in macrophages. We characterized several clinically approved and widely used fenamate NSAIDs as NLRP3 inhibitors. Flufenamic acid and mefenamic acid were efficacious in rodents in vivo in NLRP3-dependent models of inflammation in an air pouch and the peritoneum. We also show protective and therapeutic effects of the fenamates using a model of amyloid beta (Aβ)-induced memory loss, and a transgenic mouse model of AD. These data suggest that fenamate NSAIDs could be repurposed as NLRP3 inflammasome inhibitors for the treatment of AD. In addition to drug repurposing we are also actively generating novel inhibitors of the NLRP3 inflammasome, and identifying lifestyle factors that contribute to increased NLRP3-dependent inflammation in AD.

Stella Hartley

Stella Hurtley obtained her first degree in Natural Sciences at Cambridge, and then went on to PhD in Cell Biology at the European Molecular Biology Laboratory in Heidelberg. After post-docs in Yale, Philadelphia and Edinburgh, Stella joined Science at the newly established Europe office in 1994.... Read more

Stella Hurtley obtained her first degree in Natural Sciences at Cambridge, and then went on to PhD in Cell Biology at the European Molecular Biology Laboratory in Heidelberg. After post-docs in Yale, Philadelphia and Edinburgh, Stella joined Science at the newly established Europe office in 1994. As Senior Editor at the journal, Stella is responsible for looking after submissions in a variety of subject areas including Cell Biology, Prion Biology and Cellular Microbiology, and is responsible for the This Week in Science page.

Mark Cooper

Mark Cooper
Dr Mark Cooper trained in the field of mitochondrial biochemistry in disease under the supervision of Dr John Morgan-Hughes and Professor John Clark (PhD 1987) at the Institute of Neurology, London. Dr Cooper was appointed as Lecturer in the Department of Protein and Molecular Biology... Read more

Mark Cooper
Dr Mark Cooper trained in the field of mitochondrial biochemistry in disease under the supervision of Dr John Morgan-Hughes and Professor John Clark (PhD 1987) at the Institute of Neurology, London. Dr Cooper was appointed as Lecturer in the Department of Protein and Molecular Biology at the Royal Free Hospital Medical School, and subsequently in 1994 as Senior Lecturer in the department of Clinical Neurosciences. In 2010 he was appointed as Reader in Neurodegenerative diseases in the department of Clinical Neurosciences, UCL Institute of Neurology.
Dr Cooper’s work on Parkinson’s Disease (PD) focuses on elucidating the cell and molecular mechanisms underlying the disease. Over the past 20 years his research has focussed on the role of mitochondrial dysfunction in PD brains (Schapira et al 1990) and platelets (Krige et al 1994) and its relationship to other features detected in PD brains including: mitochondrial DNA defects (Gu et al 1998), nitric oxide (Cleeter et al 1994), oxidative stress (Seaton et al 1997), iron (Hartley et al 1993) and cell death (Hartley et al 1994). Increasingly with the identification of the familial causes of PD his research has turned to the role of specific mutant genes in PD pathogenesis. Alpha-synuclein has been the main focus of his research with additional interests in: LRRK2 (Papkovskaia et al 2012), parkin (Gegg et al 2010) and glucocerebrosidase (Gegg et al 2012). While mitochondrial biochemistry is a recurrent theme he also has a broader interest in dopamine metabolism (Tabrizi et al 2000), protein degradation pathways (Alvarez-Erviti et al 2010), alpha-synuclein aggregation and transmission (Alvarez-Erviti et al 2011) and microRNA dysregulation (Alvarez-Erviti et al 2013). Dr Mark Cooper is also interested in Friedreich’s Ataxia, Huntingdon’s disease and mitochondrial abnormalities.

The 7th Oxford Genomics Forum is a 1-day event which takes place on the Wednesday 13th July at the University of Oxford’s Old Road Campus.
This year the Forum is held in partnership between the Oxford Genomics Centre and Biotexcel as a new platform to bring together genomic researchers from... Read more

The 7th Oxford Genomics Forum is a 1-day event which takes place on the Wednesday 13th July at the University of Oxford’s Old Road Campus.
This year the Forum is held in partnership between the Oxford Genomics Centre and Biotexcel as a new platform to bring together genomic researchers from diverse areas to discuss the latest advances, technologies, tools and directions in Genomics. This new platform will evolve into a full 2-day event in 2017 so join us this year and be part of the community as we take the popular forum to a new level.
The scientific theme of the forum will cover the following areas:
Technological advancement in Single Cell
Genomic Medicine
Epigenetics
Gene Regulation
Pathogenic Organisms
Cancer
Data analysis and handling
The Forum will consist of 3 keynote talks given by opinion leaders who will then chair sessions of short talks by key figures in those areas. There will also be plenty of opportunities for delegates to brainstorm ideas and discuss topics that are making the genomic headlines.
A Panel Debate and a networking discussion will allow our experts and attendees to interact and ponder over topical issues and bottlenecks such as how NGS labs are coping with the data deluge.
WHO SHOULD ATTEND THIS NGS EVENT?
All NGS users, researchers and students in genomics
Bioinformaticians
NHS & Private Labs, Biotech Companies, CRO’s, Service Providers
… and all those interested in the latest developments of:
Bioinformatics
Biomarkers
Computational Biology
Data Analysis
Data interpretation
DNA Sequencing
Genetics/Genomics
Infectious and Inherited Diseases
Informatics
Molecular and Cell Biology
Molecular Diagnostics
Next Generation Sequencing

Florent Ginhoux

Florent Ginhoux graduated in Biochemistry from the University Pierre et Marie CURIE (UPMC), Paris VI, obtained a Masters degree in Immunology from the Pasteur Institute in 2000 and his PhD in 2004 from UPMC, Paris VI. As a postdoctoral fellow, he joined the Laboratory of Miriam Merad in the Mount... Read more

Florent Ginhoux graduated in Biochemistry from the University Pierre et Marie CURIE (UPMC), Paris VI, obtained a Masters degree in Immunology from the Pasteur Institute in 2000 and his PhD in 2004 from UPMC, Paris VI. As a postdoctoral fellow, he joined the Laboratory of Miriam Merad in the Mount Sinai School of Medicine (MSSM), New York. In 2008, he became an Assistant Professor in the Department of Gene and Cell Medicine, MSSM and member of the Immunology Institute of MSSM. He joined the Singapore Immunology Network (SIgN), A*STAR in May 2009 as a Junior Principal Investigator. He is now a Senior Principal Investigator and an EMBO Young Investigator and his laboratory is focusing on the ontogeny and differentiation of macrophages and dendritic cells in both humans and mice.

Prof Kay Gruenewald, Simonas Masiulis, Michael Grange

Spotlight on CryoEM is the final seminar of the current series.
Hosted by Prof. Kay Grünewald with talks by Simonas Masiulis, “Single particle cryoEM of a GABA neurotransmitter receptor”
and Michael Grange, “CryoEM of dynein-based intracellular transport”.

Spotlight on CryoEM is the final seminar of the current series.
Hosted by Prof. Kay Grünewald with talks by Simonas Masiulis, “Single particle cryoEM of a GABA neurotransmitter receptor”
and Michael Grange, “CryoEM of dynein-based intracellular transport”.

Dr Catherine Motngomery

Adaptive design clinical trials have seen a marked increase in popularity in recent years. This has been evinced most recently by their use in the 2014 Ebola epidemic and their ongoing methodological elaboration in oncology. In this seminar, I will explore how change in the ‘gold standard’ of... Read more

Adaptive design clinical trials have seen a marked increase in popularity in recent years. This has been evinced most recently by their use in the 2014 Ebola epidemic and their ongoing methodological elaboration in oncology. In this seminar, I will explore how change in the ‘gold standard’ of the RCT – namely a move from standard to adaptive designs – is being rationalised, legitimised and popularised. Drawing on Adams et al’s (2009) conceptual framework of anticipation, I will argue that changing discourses of time and patienthood have facilitated a move away from standardization as the singular logic of trials towards an appreciation of flexibility, undergirded by probabilistic methodologies. Within this evolving moral economy of medical research, modes of knowledge production which claim to know the future are supplanting the traditional certainties of fixed and standardized experimental designs. I will explore some of the practical and theoretical implications of this for trialists, patients and drug regulators.

Gayle Peterson

Ms Peterson is an Associate Fellow of the Said Business School and Senior Managing Director for pfc social impact advisors. Ms Peterson is focused on women and children and is examining how to connect the top trillion in resources with the bottom billion around the world who live in poverty in a... Read more

Ms Peterson is an Associate Fellow of the Said Business School and Senior Managing Director for pfc social impact advisors. Ms Peterson is focused on women and children and is examining how to connect the top trillion in resources with the bottom billion around the world who live in poverty in a way that is ethical and effective. Currently, she is researching, writing and putting together an executive education curriculum about these issues to share best and next business practices with business and philanthropic executives to give them the tools they need to create scalable and sustainable change.

Professor Elizabeth Stokoe

What sort of communication skills should medical and health professionals be taught to develop and assessed on? What informs decisions about the guidance that informs communication training manuals? And does simulation or role-play work for training and assessment? I will address these questions in... Read more

What sort of communication skills should medical and health professionals be taught to develop and assessed on? What informs decisions about the guidance that informs communication training manuals? And does simulation or role-play work for training and assessment? I will address these questions in my talk. I will describe conversation analysis, as a method for analysing real encounters and identifying what works and what is less effective in communication. I will show how conversation analytic research findings underpin a training approach I have developed called the ‘Conversation Analytic Role-play Method’ (CARM). Drawing on a wide range of settings, from dating, police interviews, sales and hostage negotiation – as well as healthcare encounters – I will argue that what we think we know about talk is often wrong, and what works can be found in the tacit expertise displayed in actual interaction between professionals and their clients, patients and service users.